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PubMedDate not supplied

Influence of magnesium on the secretion and action of parathyroid hormone.

The interactions of serum levels of magnesium and parathyroid hormone (PTH) have been studied in a patient with hypomagnesemia and hypocalcemia following intestinal bypass surgery for obesity. When serum magnesium was low serum PTH was not stimulated by hypocalcemia. With correction of magnesium deficiency hypocalcemia was associated with elevation of serum PTH levels. Infusion of exogenous PTH induced a clearly detectable renal response in the presence of hypomagnesemia but the response was diminished when serum magnesium was elevated. In this patient it appears that hypomagnesemia suppressed parathyroid gland activity, leaving the renal action of PTH intact.

Calcium↗
PubMed1986

Separation of inhibitory activity from biologically active parathyroid hormone in patients with pseudohypoparathyroidism type I.

Patients with pseudohypoparathyroidism type I have the symptoms of hypoparathyroidism despite elevated levels of immunoreactive parathyroid hormone (PTH). However, the circulating levels of bioactive PTH, as measured in a cytochemical bioassay, are generally within the normal range suggesting that the high levels of immunoreactive PTH are either due to the presence of biologically inactive fragments of parathyroid hormone or to the presence of an 'inhibitor' of PTH bioactivity. Gel-permeation chromatography has been used to fractionate plasma from patients with pseudohypoparathyroidism type I and revealed the presence of high levels of bioactive PTH and of an 'inhibitor'. This inhibitory activity was absent or much lower in plasma from control subjects. These results indicate, therefore, that in pseudohypoparathyroidism type I the expression of the biological activity of PTH at the level of the kidney is affected by the presence of a circulating inhibitor which can be separated from intact PTH by gel-permeation chromatography.

Adolescent↗
PubMed2002

New point-of-care intraoperative parathyroid hormone assay for intraoperative guidance in parathyroidectomy.

The use of the intraoperative parathyroid hormone assay (QPTH) to guide a limited parathyroidectomy in patients with sporadic primary hyperparathyroidism (SPHPT) is well established. The advantage of having this assay performed in the operating room is immediate feedback for (1) confirming the complete excision of all hyperfunctioning parathyroid(s); (2) differential jugular venous sampling for localization; and (3) diagnosing suspected tissue without histopathology. For these reasons, the reliability of the hormone measurement and a short assay turnaround time are essential for surgical guidance. We report our experience using a new "point-of-care" assay for intact parathyroid hormone (iPTH). A new two-site chemiluminescent immunometric assay was used. The antibodies are inside a microtiter well, where the iPTH is measured by a strip luminometer after incubation for 5 minutes. Sixteen frozen samples were measured simultaneously using the traditional iPTH assay and this new assay for comparison. Fifty-one patients with SPHPT underwent parathyroidectomy guided by this new assay. The criteria used to predict postoperative normocalcemia was a drop in the hormone level of < or = 50% from the highest preincision or preexcision levels at 10 minutes after excision of all hypersecreting gland(s). The correlation between the traditional and new assays was 0.98. The assay predicted the postoperative calcium levels in all patients except one (false negative-delayed drop). The assay turnaround time was 8 minutes. This new point-of-care assay is reliable for predicting postoperative calcium levels when used with the described criteria. It has advantages over the traditional assay in that it is faster and easier to perform.

Humans↗
PubMed1994

Parathyroid hormone related protein (PTHrP) gene expression in fetal and extra-embryonic tissues of early pregnancy.

Parathyroid hormone related protein (PTHrP) is an important humoral factor in hypercalcaemia of malignancy. In addition there is increasing evidence that this peptide has a physiological role in fetal development, especially in cellular growth and differentiation. Both in-situ hybridization and immunohistochemistry were used together and for the first time to identify sites of PTHrP gene expression and peptide in fetal and extra-embryonic tissues of first trimester human pregnancy. PTHrP mRNA and peptide were identified in the avascular amnion and the syncytiotrophoblast while mRNA alone was expressed in the cytotrophoblast. Its expression in these extra-embryonic tissues is consistent with postulated roles for PTHrP in implantation, relaxation of endometrial muscle and regulation of vascular tone. Expression of both mRNA and peptide occurred in endo-, meso- and ectodermal structures of the fetus, consistent with local production of the peptide rather than cellular uptake from amniotic fluid and supporting a role for PTHrP in cellular growth and differentiation.

Cell Differentiation↗
PubMed1994

The effect of parathyroid hormone and other metabolic factors on extrarenal acid buffering.

Parathyroid hormone (PTH) is an 84-amino acid, a polypeptide hormone which acts in many tissues. In the human there are many clinical examples of both primary and secondary PTH excess states; while deficiency states also occur, they are far less common. This manuscript reviews the effects of PTH on extrarenal acid buffering and discusses the possible mechanisms which are involved.

Acid-Base Equilibrium↗
PubMed1995

[Regulation of parathyroid hormone in molecular biological aspect].

The synthesis of human parathyroid hormon (PTH) is controlled by extracellular Ca2+ concentration and 1,25 (OH)2D3, independently, nCaRE (negative calcium responsive element) and nVDRE (negative vitamin D responsive element) have been detected on 5' flanking region of human PTH gene. And also gene mutations of PTH in hereditary hypoparathyroidism was discovered in hereditary hypoparathyroidism.

Animals↗
PubMed1997

Immunocytochemical expression of parathyroid hormone related protein (PTHrP) in odontogenic jaw cysts.

OBJECTIVE: To investigate the immunocytochemical expression of parathyroid-hormone-related protein (PTHrP) in odontogenic jaw cysts. DESIGN: Retrospective study of archival tissue. SETTING: University department, UK. MATERIAL: Odontogenic keratocysts (n=27), and dentigerous and radicular cysts (n=10 each). INTERVENTION: Immunocytochemistry by biotin streptavidin technique. MAIN OUTCOME MEASURE: Intensity of staining of PTHrP determined by TV image analysis. RESULTS: The epithelial linings of all the odontogenic keratocysts, 9/10 dentigerous, and 8/10 radicular cysts showed reactivity for PTHrP mainly localised to the basal and suprabasal layers. Odontogenic keratocyst linings expressed significantly higher levels of PTHrP than those of dentigerous and radicular cysts (P<0.003 in each case). There were no differences in epithelial expression of PTHrP between solitary, recurrent and naevoid basal cell carcinoma syndrome-associated odontogenic keratocysts. The fibrous tissue walls of all types of cyst reacted strongly for PTHrP with a trend towards decreasing intensity from odontogenic keratocysts, to dentigerous and then radicular cysts. CONCLUSION: It is possible that PTHrP modulates growth and bone resorption in odontogenic cysts. PTHrP may act synergistically with interleukin-1 to increase bone resorption or stimulate osteoblasts and inhibit osteoclasts (resulting in reduced resorption) via its transforming growth factor beta-like activity.

Analysis of Variance↗
PubMed2003

Both duration and degree of hypercalcemia influence the reduced parathyroid hormone response to hypocalcemia after hypercalcemia.

The stimulation of parathyroid hormone (PTH) secretion by hypocalcemia is reduced when hypocalcemia is preceded by hypercalcemia. The present study investigates whether the duration and degree of hypercalcemia influence the reduced PTH response to hypocalcemia after hypercalcemia. In addition, the implication of the arachidonic acid (AA) signaling pathway in this effect is evaluated. The PTH response to hypocalcemia has been studied in a control group and in four groups of rabbits subjected to hypercalcemia for different periods of time (between 30 and 120 min) and at two levels of hypercalcemia (1 x 9 and 2 x 1 mM). AA levels have been measured in parathyroid glands from rabbits subjected to hyper- and hypocalcemia. When compared with controls, rabbits that had been hypercalcemic (2 x 1 mM) for 2 h showed a markedly attenuated PTH response to hypocalcemia (50% of normal PTHmax), rabbits that had been in hypercalcemia (2 x 1 mM) for 75 min had an intermediate PTH response to hypocalcemia (70% of normal PTHmax) and rabbits that had been subjected to either 30 min hypercalcemia of 2 x 1 mM or 120 min hypercalcemia of 1 x 9 mM had a normal PTH response to hypocalcemia. AA levels increased in hypercalcemia and decreased in hypocalcemia; however, no differences were observed at either calcium level in short-time (30 min) versus long-time (120 min) hypercalcemia. In conclusion, the attenuated PTH response to hypocalcemia after hypercalcemia is dependent on both the period of time that the parathyroid glands have been exposed to hypercalcemia and the degree of hypercalcemia. In addition, this reduced PTH response does not seem to be related to changes in the AA signaling pathway.

Animals↗
PubMed2002

[Intraoperative monitoring of intact parathyroid hormone during surgery for primary hyperparathyroidism].

The aim of the present study was to evaluate a new immunometric assay for intraoperative parathyroid hormone monitoring. The test was applied in 70 patients who underwent surgery for primary hyperthyroidism (pHPT) between 6/1999 and 6/2001. Among these patients, 61 showed a solitary adenoma, eight a hyperplasia and one a double adenoma. Intraoperative iPTH samples were taken at the beginning of the operation and 5, 10 and 15 min after removal of the parathyroid gland. Criterion for a successful operation were a decrease of iPTH levels of more than 50 % within 5 min and of more than 60 % within 15 min after parathyroidectomy. Following the removal of a solitary adenoma, iPTH levels decreased by 63 % (+/- 13 %) after 5 min and by 76 % (+/- 10 %) after 15 min respectively. In case of hyperplasia, a significant decrease of iPTH levels was not observed until a subtotal parathyroidectomy had been carried out. In the present study there were 2 false negative and one false positive results corresponding with a sensitivity of 97 % and a specificity of 89 % for prediction of a solitary adenoma. In our opinion, intraoperative iPTH monitoring using this new assay allows the safe distinction between adenoma and multiglandular disease. It represents a valuable adjunct to surgical skill as it permits minimally invasive operations for solitary adenomas, and in case of recurrent surgery helps to detect the region of interest by selective venous sampling for parathyroid hormone.

Adenoma↗
PubMed1998

Developmental upregulation of human parathyroid hormone (PTH)/PTH-related peptide receptor gene expression from conserved and human-specific promoters.

The parathyroid hormone (PTH)/PTH-related peptide (PTHrP) receptor (PTHR) functions in skeletal development and mediates an array of other physiological responses modulated by PTH and PTHrP. PTHR gene transcription in mouse is controlled by two promoters: P1, which is highly and selectively active in kidney; and P2, which functions in a variety of tissues. P1 and P2 are conserved in human tissue; however, P1 activity in kidney is weak. We have now identified a third human promoter, P3, which is widely expressed and accounts for approximately 80% of renal PTHR transcripts in the adult. No P3 activity was detected in mouse kidney, indicating that renal PTHR gene expression is controlled by different signals in human and mouse. During development, only P2 is active at midgestation in many human tissues, including calvaria and long bone. This strongly suggests that factors regulating well conserved P2 control PTHR gene expression during skeletal development. Our results indicate that human PTHR gene transcription is upregulated late in development with the induction of both P1 and P3 promoter activities. In addition, P2-specific transcripts are differentially spliced in a number of human cell lines and adult tissues, but not in fetal tissues, giving rise to a shorter and less structured 5' UTR. Thus, our studies show that both human PTHR gene transcription and mRNA splicing are developmentally regulated. Moreover, our data indicate that renal and nonrenal PTHR gene expression are tightly coordinated in humans.

Bone and Bones↗
PubMed2004

[Effects of different human parathyroid hormone 1-34 administration on SaoS-2 cells].

OBJECTIVE: To observe the effects of different human parathyroid hormone 1-34 (hPTH1-34) administration on SaoS-2 cells, and explore the mechanism of bone formation improvement. METHODS: Each cycle covered 48 h. SaoS-2 cells were continuously or intermittently stimulated by 50 ng/ml hPTH1-34 for 1, 3, 6, 12, and 24 h in each cycle. Total RNA was extracted by Trizol kit. Alkaline phosphatase (ALP), osteocalcin or bone Gla-containing protein (BGP) and cyclic adenosine monophosphate (cAMP) levels were measured by chemical method, radioimmunoassay and competitive protein binding method, respectively. c-fos gene expression was semi-quantified by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: ALP level was time-dependently increased in 1, 3 and 6 h stimulation, especially in 3 and 6 h (compared with control, P < 0.01; P < 0.05 or P < 0.01 compared with continuous stimulation). The cAMP level was time-dependently increased in 3 and 6 h incubation (P < 0.05 compared with control and continuous stimulation). Intermittent hPTH1-34 stimulation had more effects on cAMP level than continous action (P < 0.001). hPTH1-34 intermittent stimulation of 1, 3, and 6 h enhanced c-fos gene expression time-dependently. CONCLUSIONS: Intermittent hPTH1-34 stimulation has a stronger effect on osteoblast than continuous action, especially in 3, 6 h in each cycle intermittent stimulation. The synchronous responses of c-fos, ALP and cAMP to hPTH1-34 suggest that hPTH1-34 affect Saos-2 cells through cAMP dependent protein kinase A (PKA) pathway and c-fos gene paly an important role.

Alkaline Phosphatase↗
PubMed2006

Intraoperative parathyroid hormone measurement during minimally invasive parathyroidectomy: does it "value-add" to decision-making?

BACKGROUND: Routine use of intraoperative parathyroid hormone levels (IOPTH) during minimally invasive parathyroidectomy (MIP) has been challenged simply because the test works best when needed least, ie, once a solitary adenoma has been resected, and is less accurate with multiple gland disease. It has also been shown not to be cost-effective. The aim of this study was to determine if IOPTH "value-added" to decision-making during MIP. STUDY DESIGN: The study group comprised 100 consecutive patients with sporadic hyperparathyroidism and an unequivocally positive sestamibi scan who were undergoing MIP in our unit from June 2004 until October 2005, from whom blood was collected for parathyroid hormone measurement preoperatively, preexcision, and at 10 and 30 minutes postremoval. No action was taken on the results of the test. RESULTS: Ninety-eight patients were cured by MIP alone. Two patients had persistent hyperparathyroidism, one of whom was cured with subsequent open reexploration and removal of a second adenoma, and the other remains hypercalcemic despite additional open neck exploration. IOPTH in both patients failed to fall in retrospect, only the first would have been cured by conversion at the time of operation. The value-added accuracy of IOPTH was really only 1%. In an additional nine patients, IOPTH at 10 minutes had failed to fall by > 50% from the highest level, those patients (9%) would have been subjected to an unnecessary conversion on the basis of a false-negative result. CONCLUSIONS: IOPTH does not substantially value-add to decision-making during MIP. Most patients will be cured with appropriate selection for MIP based on preoperative localization studies.

Adult↗
PubMed1980

The long-term effect of lowering dialysate magnesium on circulating parathyroid hormone in patients on regular haemodialysis therapy.

Measurement of parathyroid hormone (PTH) in a group of patients on regular dialysis therapy (RDT) showed little acceleration of the development of raised concentrations until the dialysate concentration of magnesium was halved from 0.5 to 0.25 mmol/l. Patients with sustained concentrations of PTH changed less than those who were within the normal range at the outset.

Adult↗
PubMed1993

Alcohol-induced bone disease: relationship to age and parathyroid hormone levels.

Alcohol abuse leads to osteopenia and fractures. Epidemiological evidence suggests that older alcoholics are at substantially greater risk of fractures than younger alcoholics. To examine the interaction of age and alcohol abuse on bone mineral homeostasis, we studied 27 subjects with a history of 10 more years of alcohol abuse ranging in age from 26-68 years. They were evaluated for disordered bone mineral homeostasis by assessing bone density (by quantitative computed tomography of the lumbar spine), histomorphometry of a transcortical biopsy from the iliac crest, serum levels of vitamin D metabolites and parathyroid hormone, and serum and urine levels of bone minerals. Seventeen of the subjects were found to have spinal compression fractures by routine radiologic procedures. The older the subject the more likely the subject was to have such a fracture. Bone densitometry indicated a marked reduction in spinal bone density with 15 subjects below 2 SD of normal aged-matched controls. Bone density fell sharply with the age of the subject. Histomorphometry of iliac crest bone biopsies revealed no evidence of osteomalacia, but total resorption surfaces were increased. Consistent with the lack of osteomalacia were the normal levels of the vitamin D metabolites. The increased total resorption surfaces were correlated with high normal or elevated levels of parathyroid hormone as indicated both by radioimmunoassay and by urinary cAMP levels. Bone formation and active bone resorption (resorption surfaces containing osteoclasts) did not correlate with parathyroid hormone levels, however, but correlated negatively with age.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1979

The control of liver regeneration by calcitonin, parathyroid hormone and 1 alpha,25-dihydroxycholecalciferol.

Removal of the thyroid in normocalcemic rats with functional parathyroid transplants was found to reduce the hepatocyte DNA synthetic activity which normally follows partial hepatectomy. This proliferative incapacitation of hepatocytes appeared to be due specifically to a calcitonin deficiency since it was overcome by a single injection of pure synthetic salmon calcitonin shortly after partial hepatectomy. Salmon calcitonin and bovine parathyroid hormone were equally able to reverse the similar proliferative incapacitation of hepatocytes in hypocalcemic rats which had both their parathyroid and thyroid glands removed one day before partial hepatectomy. However, these two hormones (individually or together) could not reverse the proliferative incapacity resulting from a more prolonged (3-day) exposure to the hypocalcemic conditions in thyroparathyroidectomized rats, but the proliferative incapacity could be reversed by simultaneous treatment with the vitamin D3 metabolite, 1 alpha,25-dihydroxycholecalciferol. We suggest that extracellular calcium ions are the actual regulators of this hormonally-controlled hepatocyte proliferative development and that parathyroid hormone and the vitamin D3 metabolite affect proliferation indirectly by determining the extracellular calcium concentration, while calcitonin directly, or indirectly, sensitizes hepatocytes to the action of calcium.

Animals↗
PubMed1990

Source of urinary cyclic AMP in response to calcitonin and parathyroid hormone in the rat.

Administration of calcitonin (CT) or parathyroid hormone (PTH) in rats, induced phosphaturia with a concomitant increase in urinary excretion of cyclic AMP. CT produced a rise in arterial cAMP and filtered cAMP, with no increase in urinary nephrogenous cAMP. PTH on the other hand, produced an elevation in urinary nephrogenous cAMP with no increase in arterial cAMP and filtered cAMP. These results indicate that the source of urinary cAMP after CT is non-renal, whereas after PTH it is renal in origin.

Animals↗